Background <p>Understanding how a disease develops and the factors that influence any deviation from the balance created by the body is critical in tailoring appropriate treatment for each patient. Existing literature discusses each factor separately, and simply touches on the interaction by recognizing its existence. The objective of this study is to delve in to the relationship between the immune system and the gut microbiota, and how they in turn affect each other and ultimately lead to a diseased state.</p> Methods <p>To locate relevant published research, a comprehensive search of electronic databases was performed. Eligible studies were chosen based on predetermined inclusion criteria, which included original research publications exploring the link between the immune system and gut microbiome in IBD patients. Data extraction and quality evaluation followed the PRISMA recommendations. The included studies used a variety of techniques, including observational cohort studies, case–control studies, and experimental research.</p> Results <p>Changes in systems from homeostatic function include a dysregulated immune response with heightened pro-inflammatory cytokines, disrupted gut barrier permeability due to increased epithelial permeability and disrupted tight junctions, reduced microbial diversity with elevated levels of pathogenic strains and bacteriophages. Short-chain fatty acids which promote gut barrier integrity and possess anti-inflammatory effects are reduced in patients with IBD.</p> Discussion <p>Key findings from the literature review emphasize the role of gut microbiota in immunological responses in IBD, as well as the reciprocal impact of immune dysregulation on microbiome composition. Further research is needed to understand the molecular interaction between the immune system and the gut microbiota (Caron et al. in J Crohns Colitis 18:ii3–ii15, 2024. <a href="https://doi.org/10.1093/ECCO-JCC/JJAE082">https://doi.org/10.1093/ECCO-JCC/JJAE082</a>).</p>

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A systematic review on the dynamic interplay between the immune system and gut microbiome in inflammatory bowel disease patients

  • Danah Almusallam,
  • Samiah Alhabardi

摘要

Background

Understanding how a disease develops and the factors that influence any deviation from the balance created by the body is critical in tailoring appropriate treatment for each patient. Existing literature discusses each factor separately, and simply touches on the interaction by recognizing its existence. The objective of this study is to delve in to the relationship between the immune system and the gut microbiota, and how they in turn affect each other and ultimately lead to a diseased state.

Methods

To locate relevant published research, a comprehensive search of electronic databases was performed. Eligible studies were chosen based on predetermined inclusion criteria, which included original research publications exploring the link between the immune system and gut microbiome in IBD patients. Data extraction and quality evaluation followed the PRISMA recommendations. The included studies used a variety of techniques, including observational cohort studies, case–control studies, and experimental research.

Results

Changes in systems from homeostatic function include a dysregulated immune response with heightened pro-inflammatory cytokines, disrupted gut barrier permeability due to increased epithelial permeability and disrupted tight junctions, reduced microbial diversity with elevated levels of pathogenic strains and bacteriophages. Short-chain fatty acids which promote gut barrier integrity and possess anti-inflammatory effects are reduced in patients with IBD.

Discussion

Key findings from the literature review emphasize the role of gut microbiota in immunological responses in IBD, as well as the reciprocal impact of immune dysregulation on microbiome composition. Further research is needed to understand the molecular interaction between the immune system and the gut microbiota (Caron et al. in J Crohns Colitis 18:ii3–ii15, 2024. https://doi.org/10.1093/ECCO-JCC/JJAE082).